IL-1 receptor regulates S100A8/A9-dependent keratinocyte resistance to bacterial invasion

B. S. Sorenson, Ali Khammanivong, B. D. Guenther, Karen F Ross, Mark C Herzberg

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Previously, we reported that epithelial cells respond to exogenous interleukin (IL)-1α by increasing expression of several genes involved in the host response to microbes, including the antimicrobial protein complex calprotectin (S100A8/A9). Given that S100A8/A9 protects epithelial cells against invading bacteria, we studied whether IL-1α augments S100A8/A9-dependent resistance to bacterial invasion of oral keratinocytes. When inoculated with Listeria monocytogenes, human buccal epithelial (TR146) cells expressed and released IL-1α. Subsequently, IL-1α-containing media from Listeria-infected cells increased S100A8/A9 gene expression in nave TR146 cells an IL-1 receptor (IL-1R)-dependent manner. Incubation with exogenous IL-1α decreased Listeria invasion into TR146 cells, whereas invasion increased with IL-1R antagonist. Conversely, when S100A8/A9 genes were knocked down using short hairpin RNA (shRNA), TR146 cells responded to exogenous IL-1α with increased intracellular bacteria. These data strongly suggest that infected epithelial cells release IL-1α to signal neighboring keratinocytes in a paracrine manner, promoting S100A8/A9-dependent resistance to invasive L. monocytogenes.

Original languageEnglish (US)
Pages (from-to)66-75
Number of pages10
JournalMucosal Immunology
Volume5
Issue number1
DOIs
StatePublished - Jan 1 2012

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Interleukin-1 Receptors
Interleukin-1
Keratinocytes
Epithelial Cells
Listeria
Listeria monocytogenes
Leukocyte L1 Antigen Complex
Bacteria
Gene Expression
Cheek
Interleukins
Small Interfering RNA
Genes

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IL-1 receptor regulates S100A8/A9-dependent keratinocyte resistance to bacterial invasion. / Sorenson, B. S.; Khammanivong, Ali; Guenther, B. D.; Ross, Karen F; Herzberg, Mark C.

In: Mucosal Immunology, Vol. 5, No. 1, 01.01.2012, p. 66-75.

Research output: Contribution to journalArticle

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